Transcript Amanitax - UNM Biology

Group Project
Amanita Mushrooms
Toxins
Ahmed Alghrouz
Ali Ahmed
James Olguin
Tristan Malin
Start
Amanita Mushrooms
History & Background
Species:

A. muscaria (Fly Agaric)

A. phalloides (Death Cap)

A. virosa (Destroying Angel)
References
History & Background
 Introduction: A history of interaction.
 Timeline
 Psychoactive Compounds
 Neuropharmacology of Psychoactive Amanita Compounds
 References
Back to Amanita Homepage
A History of Interaction
 A. muscaria has been proposed as the true entity
behind Soma, the apple in the Garden of Eden, the
apples of Hesperides, the Golden Fleece, the fire of
Prometheus, Kakulja kurakan ‘Lightning bolt One-leg’
of the Mayans, the Huitzilapochtli aspect of
Tezcatlipoca of the Aztecs, Jesus Christ, and Santa
Claus. (Hajicek-Dobberstein 1995)
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Back to History & Background
 In today’s modern culture: A.
muscaria makes appearances in
gnome and fairy
folklore/ornaments, in Alice in
Wonderland, the Smurfs,
Disney’s Fantasia, and the Super
Mario Bros franchise.
Back to History & Background
Timeline
 The use of A. muscaria began sometime after the last
Ice Age in the northern Eurasian forest belt and spread
north following the retreating polar ice cap,
approximately 9,000 BCE. (Wasson 1968)
 5,000-3,000 BCE: Earliest linguistic evidence of known
intoxication from ingestion of A. muscaria.
 ~4000 BCE: The Uralic language split into two branches,
containing similar root words for inebriation. The root
"pang" signifies both 'intoxicated' and the A. muscaria.
(Wasson 1968)
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 1000-2000 BCE: Petroglyphs along the Pegtymel River in
north eastern Siberia.The Chukchi culture, the areas current
inhabitants, are known to have used A. muscaria. (Ott 1996)
 1200 BCE: Rg Veda hymns mention a magical intoxicant called
Soma.
 In 1968, R. Gordon Wasson published Soma: Divine Mushroom
of Immortality, arguing that Soma refers to A. muscaria.
Back to History & Background
Next
 100 CE: 7.5 cm tall
miniature statue of an
A. muscaria, found in
Nayarit, Mexico.
 1250 CE: Albertus
Magnus describes the
insecticidal properties
of A. muscaria, in De
vegetabilibus. (Letcher
2007)
 These properties led
to the common name
"fly agaric".
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Back to History & Background
 1291 CE: Art
historians argue that
this is a
conventionalized
tree type, prevalent
in Romanesque and
early Gothic art,
referred to as a
"mushroom tree".
(Wasson 1968)
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Back to History & Background
 1658 CE: Polish prisoner of war writing about a culture
from western Siberia (Ob-Ugrian Ostyak of the Irtysh
region): "They eat certain fungi in the shape of flyagarics, and thus they become drunk worse than on
vodka, and for them that's the very best banquet."
(Wasson 1968)
 Originally published in Kamiensky Dluzyk. Diary of
Muscovite Captivity (1874) pg 382.
 1730 CE: Swedish Colonel Filip Johann von
Strahlenberg gives detailed descriptions of Siberians
consuming tea made from A. muscaria and drinking
the urine of those who previously ingested the
mushroom, recycling the intoxicating ingredients.
(Wasson 1968)
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Back to History & Background
 1753 CE: Linnaeus describes the fly agaric mushroom
in Species Plantarum: Tomus II. Holmiae (1753),
naming it Agaricus muscarius.
 1783 CE: Fly agaric placed in Amanita genus by JeanBaptiste Lamarck.
 New name Amanita muscaria.
 1968 CE: R. Gordon Wasson publishes Soma: Divine
Mushroom of Immortality. (Argument for sacramental use
of A. muscaria by Indians in time of Vedas.)
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Back to History & Background
 1972 CE: Robert Graves, in Difficult Questions,
Easy Answers, proposes that the character of Santa
Claus may be based on A. muscaria shamanism.
 Jonathan Ott later develops this in his book
Hallucinogenic Plants of North America (1976).
 2002 CE: Clark Heinrich, in Magic Mushrooms in
Religion and Alchemy (2002), argues that A. muscaria
has played a large role in the worlds largest religions
including: Hinduism, Judaism, and Christianity.
Back to History & Background
Psychoactive Compounds
 The primary active chemicals known in Amanita
muscaria and A. pantherina are: Muscimol, Ibotenic
Acid, and Muscarine.
 There are other chemicals present in trace amounts,
below active levels in humans.
 The pharmacology of A. muscaria is not fully
understood.
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Back to History & Background
Muscimol
 Muscimol is considered the principle psychoactive,
with oral dosages of pure muscimol around 10-15
milligrams. (Spinella 2001, Ott 1996)
 Muscimol is a potent, selective agonist of the GABA
receptor.
 Muscimol is the product of the decarboxylation of
ibotenic acid.
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Back to History & Background
Ibotenic Acid
 Ibotenic acid, another psychoactive compound, is also
active orally, but at doses 5-8 times higher than those
of muscimol. (Ott 1996, Schultes 1980)
 Shown to be highly neurotoxic by injection directly
into mice and rat brains, it is a powerful brainlesioning agent. (Spinella 2001)
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Back to History & Background
Muscarine
 Muscarine was the first parasympathomimetic
substance ever studied.
 By mimicking acetylcholine, it causes profound
activation of the peripheral parasympathetic
nervous system resulting in convulsions and
possible death.
 Muscarine is present only in trace amounts in A.
muscaria.
Back to History & Background
Neuropharmacology of
Psychoactive Amanita compounds
 Muscimol and Ibotenic Acid are both psychoactive.
 First let us examine GABA, the primary pathway
affected by ingestion of these compounds.
Next
Back to History & Background
GABA
 GABA (gamma-aminobutyric acid) was first
described as a plant and microbe metabolic
product, and later identified as integral to the
mammalian central nervous system.
 In the hippocampus and neocortex, GABA is
primarily excitatory in early development,
regulating growth, migration, and elongation of
neural progenitor cells and the formation of
synapses.
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Back to History & Background
 In adult mammals, GABA is the main inhibitory
neurotransmitter, playing an important role in
regulating the nervous system.
 Agonizing GABA receptors in mammals typically
results in calming, anti-anxiety, and anti-convulsive
effects.
 GABA works by binding to specific receptors in the
plasma membranes of pre- and post-synaptic neurons,
and causes hyperpolarization.
 Three types of receptors: GABAA and GABAC are
ionotropic receptors (are ion channels) and GABAB
metabotropic, which are G-protein coupled.
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Back to History & Background
Muscimol
 Muscimol is a potent agonist of the GABAa, altering
and inhibiting neural activity in the cerebral cortex,
hippocampus, and cerebellum.
 In vivo, muscimol will pass through the human body
and excreted in the urine as muscimol.
Next
Back to History & Background
Ibotenic acid
 When ingested, a small portion is decarboxylated into
muscimol, which is the psychoactive effective portion.
 Ibotenic acid is used clinically as a brain lesioning
agent.
 Described by Olpe et al. 1978.
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Back to History & Background
Intoxicating Effects
 The effects of the ingestion of muscimol are often
described as unstructured hallucinations, likened
to a lucid dream state.
 Effects felt include: visual distortion,
hallucination, loss of equilibrium, muscle
twitching, and altered sensory perception.
 Effects last 6-8 hours, peaking 2-3 hours after
ingestion. However, this is dose sensitive, and
potency varies between mushrooms.
Back to History & Background
Amanita Virosa
(The Destroying Angel)
 Taxonomy / Taxonomic Confusion
 Description
 Distribution / Habitat
 Toxins
 Symptoms / Treatment
Back to Amanita Homepage
Taxonomy
Kingdom: Fungi
Phylum: Basidiomycota
Class: Agaricomycetes
Order: Agaricales
Family: Amanitaceae
Genus: Amanita
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Back to A. virosa
Taxonomic Confusion
Depending on the source, one or more species of
Amanita mushroom are considered to be death
angels. However, the general consensus is that there
are three types of mushrooms that fit the category.
They are: A. bisporiga, A. ocreata, and A. virosa.
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Taxonomic Confusion
One method used to define the destroying angel is the
potassium hydroxide test (KOH test). When a
destroying angel comes into contact with KOH, its
flesh turns yellow. One source of taxonomic confusion
is that mushrooms, incorrectly labeled as one of the
destroying angels, have tested negative on the KOH
test, therefore casting doubt on their classification.
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Back to A. virosa
KOH Test
An image of the yellow flesh, that is the result of
application of Potassium Hydroxide
Back to A. virosa
Next
Taxonomic Confusion
A. verna has at times also been included in the category
of destroying angel, however, this is not generally
considered to be the case. For the purposes of this
slide show, the category of destroying angel will
include A. bisporiga, A. virosa, and A. ocreata only.
Back to Destroying Angel
Back to A. virosa
Description
All destroying angels form ectomycorrhizal relationships
with tree roots.
Next
Back to A. virosa
Description
Young destroying angels are often spherical or conical in
shape, until they emerge through the universal veil.
A. virosa at
three
different
stages of
life.
Next
Back to A. virosa
Description
Other identifying characteristics
of destroying angels are the
partial veil, which forms a ring
on the upper stalk, free gills
(unattached to stalk), and the
volva, or the remnants of the
universal veil, found near the
base of the mushroom.
Back to Destroying Angel
Back to A. virosa
Distribution
A. virosa occurs all over North America, Europe
A map of the
distribution of
A. ocreata, a
geographically
limited species.
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Back to A. virosa
Habitat
Like most fungi, destroying
angels tend to grow in moist,
low light conditions. They
grow near and around trees,
and forests, and their
mycelium (a structure
resembling roots) interact
with the tree roots.
Back to A. virosa
Next
Habitat
The destroying angel’s mycorrhizal relationship with
tree roots is a symbiotic one. The fungus supplies the
tree with phosphorous, while the tree nourishes the
fungus with sugars.
Glucose molecules
Back to A. virosa
Back to Destroying Ange
Toxins
Destroying angels produce and maintain two types of
toxins: amatoxins and phallotoxins. Amatoxins are
considered to be the more dangerous of the two,
because phallotoxins are not absorbed through the
gastrointestinal tract. In fact, many commonly eaten
mushrooms contain phallotoxins.
Back to A. virosa
Next
Toxins: Amatoxins
Amatoxins consist of several cyclic octapeptidal compounds,
the most toxic of which are α-amanitin and β-amanitin. αamanitin has a suspected LD50
of .1mg/kg in humans.
Name
R1
R2
R3
R4
R5
α-Amanitin
NH2
OH
OH
OH
OH
β-Amanitin
OH
OH
OH
OH
OH
γ-Amanitin
NH2
OH
H
OH
OH
ε-Amanitin
OH
OH
H
OH
OH
Amanullin
NH2
H
H
OH
OH
Amanullinic
acid
OH
H
H
OH
OH
Amaninamid
NH2
e
OH
OH
H
OH
Amanin
OH
OH
OH
H
OH
Proamanulli
n
NH2
H
H
OH
H
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Toxins: Amatoxins
Amatoxins function to inhibit
RNA polymerase II, which is
essential to the creation of
mRNA and snRNA (small
nuclear). With RNA
polymerase inhibited, it is
impossible to synthesize
proteins, and the afflicted cell
undergoes apoptosis.
Back to A. virosa
RNA polymerase II
unraveling dsDNA
Symptoms
The symptoms of Amatoxin poisoning occur in two
stages. First, vomiting, diarrhea and other GI
symptoms occur. These initial symptoms may last
around 2 – 3 days, but are not generally life
threatening.
Next
Back to A. virosa
Symptoms
After initial symptoms are resolved, the second set of
symptoms begins. Sometimes as many as 1 – 2 weeks
pass before the liver begins to fail. The afflicted
individual would experience jaundice, and in many
cases, hepatic encephalopathy, or the impairment of
brain cells due to the buildup of toxic substances
usually removed from the body by a healthy liver.
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Treatment
The only certain way to prevent death from ingestion of
a destroying angel is a liver transplant, which itself
carries no small risk. In patients that did recover from
destroying angel poisoning, as many as half suffered
from irreversible liver damage.
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Treatment
In addition to a liver transplant, there are several other
treatments that are to some degree effective. Silibinin
(from the blessed milk thistle plant) prevents the
uptake of amatoxins in hepatocytes that are not yet
damaged. One other effect of amatoxins is the
depletion of glutathione in the liver. By administering
N-acetylcysteine, a precursor to glutathione, this
exhaustion of glutathione stores can be averted.
Back to Destroying Angel
Amanita Muscaria
(Fly Agaric)
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General Facts
Description
Habitat
What people think of A.
muscaria
Toxicity
Symptoms
Treatment
References
Back to Amanita Homepage
Facts
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Also known as fly agaric or fly Amanita.
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Street names: Magic mushrooms, Liberties, magics, mushies,
liberty cap, shrooms, Amani, agaric.
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Kingdom: Fungi, Phylum: Basidiomycota, Class: Basidiomycetes, Order:
Agaricales, Family: Amanitaceae, Genus: Agaricus.
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It’s a psychoactive fungus; affects central nervous system.
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It grows in symbiosis with arboreal trees such as Birch, Pine or Fir.
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Native throughout the temperate and boreal regions of the Northern
Hemisphere.
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It’s not very toxic but it can be depending on the amount, season,
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It was used as an intoxicant and entheogen by the peoples of Siberia, India and
others throughout history and it has a religious significance in these cultures.
Amanita muscaria
Description
Pileus:
Cap 6-39 cm broad, rounded at first, then plane in age, surface viscid when
moist; margin striate often with adhering partial veil fragments when
young; cap red, usually with white warts but in some variety, yellow warts.
Lamellae:
Gills adnexed to free, white to cream, edges roughened.
Stipe:
Stipe white, 7-16 cm long, 2-3 cm thick, tapering to a bulbous base; partial
veil membranous, breaking to form a superior skirt-like veil. Volva
consisting of two to three concentric rings at the stipe base.
Spores:
Spores 9-13 x 6.5-9.5 µm elliptical, smooth, nonamyloid. Spore print white.
Amanita muscaria
Range & Habitat
 A. muscaria is native to conifer and deciduous woodlands throughout
the temperate and boreal regions of the Northern Hemisphere,
including high elevations of warmer latitudes in regions like the Hindu
Kush and the Mediterranean.
 A recent molecular study proposes an ancestral origin in the Siberian–
Beringian region in the Tertiary period before radiating outwards
across Asia, Europe and North America.
 This type of mushroom was introduced to Australia, Africa and New
Zealand with pine trees imported from Europe.
 It’s generally grows throughout the summer and early fall but in some
regions of the pacific coast it can be found in late fall and even early
winter.
Amanita muscaria
What do people think of A. muscaria?
 The effects of the mushrooms can take between 30 minutes to two hours to happen.
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The strongest part of the trip takes 4-10 hours and the after-effects usually last a further
2-6 hours. The more you take, the longer your trip could last.
Magic mushrooms can make you feel confident, relaxed and in good spirits.
They can distort color, sound and objects. One effect can be that your senses get mixed
up so that, for example, you think you can hear colors and you can see sounds.
They can also speed up and slow down your sense of time and movement. You may feel
like you're dreaming when you're awake.
You can feel more emotionally sensitive. Some people become creative and feel
enlightened.
Fly agaric (Amanita Muscaria) is risky to take.
‘Bad trips’ are seriously frightening and unsettling. And you can't tell whether you're
going to have a bad trip or a good trip. Also you can get flashbacks some time
afterwards.
You may be at risk when you’re not in complete control of what you're doing. Your
perception of your body and the world around you can be distorted.
Eating the wrong kind of mushroom can make you seriously ill, and even kill you.
Magic mushrooms can complicate any mental health issues you may have.
Amanita muscaria
Toxicity
 Muscimol: A psychoactive compound; an agonist of the
GABA receptor in the brain.
 Ibotenic acid: A powerful neurotoxin; an agonist of
NMDA glutamate receptors in the brain.
 Amanita muscaria and related species are known as
effective bioaccumulators of vanadium; some species
concentrate vanadium to levels of up to 400 times those
typically found in plants. Vanadium is present in fruitbodies as an organometallic compound called amavadine.
However, the biological importance of the accumulation
process is unknown.
Amanita muscaria
Muscimol
 Chemical Name: 5-(Aminomethyl)-3(2H)-isoxazolone
 Molecular weight: 114.10
 Muscimol is the product of the decarboxylation or drying of Ibotenic acid and
it is thought that Muscimol is as much as ten times more potent than ibotenic
acid.
 It is also a potent partial agonist at the GABAc receptor which is distributed in
different parts of the brain and highly expressed in the retina.
 Muscimol gets secreted unchanged in the urine.
 Muscimol lacks cholinergic effects at the neuromuscular junction
 LD50 mice: 3.8 mg/kg s.c, 2.5 mg/kg (I.P.)
 LD50 rats: 4.5 mg/kg (I.V.), 45 mg/kg (orally).
Mechanism
Toxicity
Amanita muscaria
Muscimol
Mechanism
• Muscimol activates the receptor for the brain's major
inhibitory neurotransmitter, GABA.
• It binds to the same binding site on the GABAa receptor
complex as GABA itself.
• It alters neural activity in multiple regions including the
cerebral cortex, hippocampus, and cerebellum. These regions
of the brain have many functions including thinking and
balance, so administering Muscimol could have an impact on
any of these higher brain functions.
Toxicity
Amanita muscaria
Ibotenic acid
 Chemical name: alpha-Amino-2,3-dihydro-3-oxo-5-iso
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xazoleacetic acid.
Molecular weight: 158.11
It is a powerful neurotoxin that is used as a brain-lesioning
agent.
Ibotenic acid is an agonist of NMDA glutamate receptors and
certain metabotropic glutamate receptors[73] which are
involved in the control of neuronal activity
Peak intoxication is reached approximately 2-3 hours after oral
ingestion.
LD5015 mg/kg (I.V.), 38 mg/kg (oral)-(mice)
LD5042 mg/kg (I.V.), 129 mg/kg (oral)-(rats)
Toxicity
Amanita muscaria
Symptoms
 Symptoms typically appear after around 30 to 90 minutes and peak within three
hours, but certain effects can last for a number of days
 Depending on habitat and the amount ingested per body weight, effects can
range including:
Nausea
Twitching
Drowsiness,
Cholinergic crisis-like effects (low blood pressure and sweating)
Auditory and visual distortions
Mood changes
Euphoria and relaxation
Ataxia
Loss of equilibrium
 In cases of serious poisoning it causes a delirium characterized by bouts of
marked agitation with confusion, hallucinations, and irritability followed by
periods of central nervous system depression.
 Seizures and coma may also occur in severe poisonings.
Amanita muscaria
Treatment
 Medical attention should be sought in cases of suspected poisoning.
 Initial treatment consists of gastric decontamination.
 If the delay between ingestion and treatment is less than four hours,
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activated charcoal is given.
Gastric lavage can be considered if the patient presents within 1 hour of
ingestion.
There is no antidote, and supportive care is the mainstay of further
treatment for intoxication.
If a patient is delirious or agitated, this can usually be treated by
reassurance and, if necessary, physical restraints.
Additionally, benzodiazepine such as diazepam or lorazepam can be
used to control combativeness, agitation, muscular overactivity, and
seizures.
Serious cases may develop loss of consciousness or coma, and may
necessitate intubation and artificial ventilation.
Amanita muscaria
•Habitat
•Description
•Symptoms
•Treatment
•Death Cap Toxins
•Mechanism of Action
•Toxicity
•Interesting Facts
•References
Back to Amanita Homepage
Habitat
 Primarily a European species, there is no evidence that
the Death Cap is native to North America
 Usually found from late September through late
October
 Has been found in Oregon, New Jersey, New York,
California, Canada, Australia, north Africa, and New
Zealand
 The Death Cap appears most commonly under oaks
but also under beeches, chestnuts, horse-chestnuts,
birches, filberts, hornbeams, pines, and spruces
Amanita phalloides
Description
 The cap is 2¼--6" (6--16 cm) wide
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The fully open caps are commonly 10-15 centimeters in diameter
The color of the cap can be pale, yellowish, or olive-green
The cap is usually sticky or slippery but sometimes dry
The gills are white, crowded together, and very finely attached to
the upper stalk
 membranous partial veil tissue extends from the edge of the cap
to the upper stalk
 The stem is white and from 5 to 15 centimeters long and 1 to 2
centimeters in diameter
 Volva(cup-like structure) encasing the base, frequently
underground or broken up.
Amanita phalloides
Symptoms
 First symptoms usually occur 6 to 12 hours after ingestion of mushroom
 Initial symptoms include: stomach pains, vomiting, diarrhea and
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dehydration. More severe symptoms include hypotension, tachycardia,
and hypoglycemia(initial symptoms usually last 2 to 3 days)
Clinical improvement occurs with supportive care. Despite the
resolution of symptoms, hepatic and renal damage is ongoing
After 2 to 3 more days, patients usually have GI disturbances once
again, accompanied by jaundice.
Other symptoms include delirium, seizures, and coma.
Patient s eventually have Liver failure along with renal failure which
lead to death
Death usually occurs one to two weeks after ingestion of mushroom
Amanita phalloides
Treatment
 There is no “antidote” for A. Phalloides poisonings
 Treatments include: a High-dose continuous intravenous
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injection of Penicillin G (Benzylpenicillin), There is some
evidence that intravenous silibinin, an extract from the blessed
milk thistle(Silybum marianum) decreases affects of ingestion, as
well as N-acetylcysteine and Thioctic acid.
Silibinin prevents the uptake of amatoxins by hepatocytes,
thereby protecting undamaged hepatic tissue
N-acetylcysteine helps to reduce liver damage.
In the most severe cases, liver transplantation is the last option.
Treatments are most effective if poisoning is immediately
diagnosed
Amanita phalloides
Death Cap Toxins
 Consist of Amatoxins and Phallotoxins
 Amatoxins are multicyclic (ring-shaped) peptides
 Consist of at least eight compounds with a similar structure, that
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of eight amino-acid rings
Amatoxins include α-amanitin, which is the chief component
and along with β-amanitin
Lead to inhibition of RNA-polymerase 2 (which is essential for
the synthesis of mRNA
Cell metabolism stops and the cells die
Organs most affected include liver and kidneys. GI tract also
affected by toxins
Phallotoxins consist of at least seven compounds, all of which
have seven similar peptide rings.
Phallotoxins have little input in the toxicity of the Death Cap.
Amanita phalloides
Mechanism of Action
 The main element of the amatoxins is alphaamanitin.
 When filtered through the kidneys, it attacks the
convoluted tubules and instead of entering the
urine,
 it is reabsorbed into the bloodstream and
recirculated, causing repeated liver and kidney
damage
 This eventually leads to liver and kidney failure.
Amanita phalloides
Toxicity
 0.1 mg/kg is the minimal lethal dose of amatoxin
for adults
-about 8mg for an 80kg person.
 30 grams (1 oz), or half a cap, of this mushroom is
enough to kill a human
 Overall mortality estimated from 5% to 40%
-This percentage is dropping due to advances in
general care and medications
 Toxicity varies from patients due to factors of
weight, age, and overall health
Amanita phalloides
Interesting Facts
 A. phalloides is one of the most poisonous of all
known toadstools
 Could have possibly lead to the deaths of Roman
Emperor Claudius and Holy Roman Emperor
Charles VI
 New studies show that ethanol diminishes effect of
toxins in mice
Amanita phalloides
References
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Kuo, M. (2001, September). Amanita phalloides . Retrieved from the MushroomExpert.Com Web site:
http://www.mushroomexpert.com/amanita_phalloides.html
Fischer , David. W. “The Death Cap Amanita phalloides The World's Most Dangerous Mushroom.” American Mushrooms. 1997.
Cornell University. 25 April, 2009 <http://americanmushrooms.com/deathcap.htm>
A. Zheleva, A. Tolekova, M. Zhelev, Z. Dobreva, K. Halacheva, S.Popova. “IN VIVO ANTIOXIDANT AND PROOXIDANT
PROPERTIES OF AMANITA PHALLOIDES MUSHROOM TOXINS.” Trakia Journal of Sciences, Vol. 3, No. 3, 2005, pp 34-38.
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^ Köppel C (1993). "Clinical symptomatology and management of mushroom poisoning". Toxicon 31 (12): 1513–40.
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